Coconut is used as tropical fruit and drink in the tropics. The antimicrobial and antiviral activity of husk fiber from coconut was reported to mainly due to the high content of phenolic compounds (Esquenazi D. et al. 2002.).
The bioactivities of coconut also included inhibitory activity against acyclovir-resistant herpes simplex virus type 1, leishmanicidal effects (Mendonça-Filho R R. et al. 2004.), protection of hemoglobin from nitrite-induced oxidation to methemoglobin (Mantena S K. et al. 2003.), and free radical scavenging activities (Alviano D S. et al. 2004.). Coconut water is the solution of coconut fruit as well as a common and natural refreshing drink with fewer side-effects reported. Coconut water is commonly used for nutritional formulation beverages and food products due to the presence of carbohydrates, vitamins, electrolytes, minerals and proteins (Santoso U. et al. 1996. and Campbell-Falck D. et al. 2000.). Besides, coconut water is also used for preservation of ovine ovarian follicles and dog semen, in vitro culture of goat primordial follicles (Figueiredo J. R. 2000. and Andrade E R. et al. 2002.), and plant tissue culture (Tiainen, T. 1993.). In addition, coconut water is reported to have inhibitory activity against human bacterial pathogens (Mandal S M. et al. 2009.) and antiulcerogenic effects (Nneli R O. and Woyike O A. 2008.).
In mammals, the skin is the largest organ of the integumentary system and plays a defensive barrier of the external pathogenic invasion. Skin inflammation has evolved as a protective response to injury, thus eliminates foreign organisms or material, and the resolution of inflammation protect us against excessive tissue injury. A failure of resolution cause chronic inflammatior, and lead to many skin diseases. In murine disease models has indicated heterogeneity of TNF receptor usage in autoimmune disease suppression versus inflammatory tissue damage, suggesting that selective TNF receptor inhibition may be advantageous to anti-TNF treatments in combating chronic inflammatory disease. (Apostolaki M, Armaka M, Victoratos P et al. 2010.) Tumour necrosis factor-alpha (TNF-α) levels in suction blister fluids and sera of psoriatic patients are correlated increases and have relationships with disease severity. (Ettehadi P. et al. 1994., Bonifati C. et al. 1994., Groves R. et al. 2004.)
Inflammation has evolved as a protective response to insult or injury, it's a primordial response that eliminates or neutralises foreign organisms or material, the resolution of inflammation encompasses the endogenous anti-inflammatory mechanisms that protect us against excessive tissue injury and promote the restoration of tissue structure and function. In fact, our well being and survival depends upon its efficiency and carefully-balanced control. In general, the innate inflammatory response initiates within minutes and, if all is well, resolves within hours. In contrast, chronic inflammation persists for weeks, months or even years. (Lawrence T. and Gilroy D. W. 2007.) In the late phase of acute inflammation, IL-10 and TGF-β will be produced to limit inflammation and promote resolution. These two cytokines (IL-10 and TGF-β) are associated with resolution of inflammation. (Lawrence T. and Gilroy D. W. 2007, Serhan C. N. et al. 2007.)
The liver plays an important role in immunological tolerance due to its anatomical location, as it links the gastrointestinal tract and the systemic venous circulation. Therefore, immune reactions against dietary or bacterial antigens from the gut have to be avoided. The function of the liver as clearance organ, however, harbors the danger that the substances that should be degraded and/or eliminated lead to tissue damage. Thus, effective defense mechanisms are necessary. Among the nonparenchymal cells Kupffer cells, sinusoidal endothelial cells, and natural killer (NK) lymphocytes exert cellular defense functions for the whole body but also for the liver itself. Furthermore, each cell type of the liver, including the hepatocytes, possesses its own defense apparatus. (Erhardt A. et al. 2010, Ramadori G. et. al. 2008.)
Rheumatoid arthritis pathology consists that synovial inflammation inside the joint capsule gives rise to a pannus, and then the pannus gradually invades the cartilage and even the surface of the bone. The immune system of patients with rheumatoid arthritis lost the ability to discriminate self from non-self. The immune system attacks synovial tissue and connective tissue in the highly movable joints of the limbs in the beginning, followed by disruption of the balance between bone formation and resorption, activating osteoclasts, and thus resulting in the destroy of articular cartilage and bone.
Because of the immunological mechanisms of rheumatoid arthritis involved in complex networks connecting a multitude of cells and cytokines, the detailed pathogenic mechanisms in rheumatoid arthritis remains unclear (Gary S. and Firestein, M. 2005.).
Pharmacologic treatments of rheumatoid arthritis and also other arthritis associated diseases, such as osteoarthritis, ankylosing spondylitis, and acute gouty arthritis, include non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, disease modifying anti-rheumatic drugs (DMARDs), and biological agents. Because arthritis is an inflammatory condition, first-line therapy is aimed to suppress inflammation and to release symptoms, such as NSAIDs and corticosteroids, which are effective in controlling the pain, swelling and stiffness related to arthritis. However, these two treatments have adverse effects and limited impact on long-term outcomes. Biological agents, such as etanercept, infliximab, and adalimumab, are often combined used with methotrexate and have also been shown to be effective in rheumatoid arthritis patients but may be considered second choice because of cost consideration. DMARDs, including methotrexate, hydroxychloroquine, sulfasalazine, leflunomide, and other antirheumatic drugs, such as gold salts and cyclosporin, are slow-acting compounds and act mainly to inhibit the proliferation of immune cells as well as to diminish the inflammation. Although DMARDs are common used for diagnosed cases of rheumatoid arthritis, reported adverse reactions and toxicities should be concerned (Gaffo A. et al. 2006., Gary S. and Firestein, M. 2003., and Gary S. and Firestein, M. 2005.).
The complexity and redundancy of the regulatory mechanisms combined with the observed interpatient variability in the disease process explains why some patients may respond to a particular therapy whereas others do not, especially when targeting pathways downstream of key regulators of immunologic events. Current drugs specifically target upstream cytokines involved in the inflammatory response of rheumatoid arthritis, include the IL-1 inhibitors (e.g. anakinra and kineret), anti-tumor necrosis factor (anti-TNF-α) agents (e.g. etanercept, infliximab, and adalimumab), the co-stimulation blocker of T cell activation (e.g. abatacept), and the selective B cell depletion agent, for example, anti-CD20 monoclonal antibody (e.g. rituximab) (Gaffo A. et al. 2006., Gary S. and Firestein, M. 2003, and Gary S. and Firestein, M. 2005.). These agents can specifically inhibit abnormal immune response thus suppress the inflammation, however, patients are also at higher risk for infection because of the immunosuppressive side-effect.
Therefore, a heretofore unaddressed need exists in the art to address the aforementioned deficiencies and inadequacies, especially in connection with coconut water extract and coconut shell extract.